Metabolic syndrome (MetS) and genetic polymorphisms PNPLA3rs738409, TM6SF2 rs58542926 and MBOAT7 rs641738 are known inductors of non-alcoholic fatty liver disease (NAFLD).
Metabolic syndrome (MetS) and genetic polymorphisms PNPLA3 rs738409, TM6SF2rs58542926 and MBOAT7 rs641738 are known inductors of non-alcoholic fatty liver disease (NAFLD).
Metabolic syndrome (MetS) and genetic polymorphisms PNPLA3 rs738409, TM6SF2 rs58542926 and MBOAT7rs641738 are known inductors of non-alcoholic fatty liver disease (NAFLD).
Chemerin and its receptor, chemokine-like receptor 1 (CmklR1), are associated with chemotaxis, inflammation, and endothelial function, especially in metabolic syndrome, coronary heart disease, and hypertension.
Chemerin and its receptor, chemokine-like receptor 1 (CmklR1), are associated with chemotaxis, inflammation, and endothelial function, especially in metabolic syndrome, coronary heart disease, and hypertension.
It was found that OA extract decreased brain infarction, neurological score, oxidative stress status, and inflammatory mediators but increased eNOS expression in the cortical area; the increased VCAM-1 and intima-media thickness together with the reduction of lumen diameter of common carotid artery of MetS eats with MCAO were also mitigated by OA extract.
The novel strategy against ischemic stroke in metabolic syndrome (MetS) targeting at oxidative stress and inflammation has gained attention due to the limitation of the current therapy.
At the end of the 5-year follow- up, compared with subjects without MS, hazard ratios and 95% confidence intervals for the different risks in subjects with MS were 1.86 (1.02-3.29) for myocardial infarction (MI), 1.39 (1.01-2.05) for stroke, 1.52 (1.02- 2.37) for CVD death, and 1.13 (0.62-2.58) for total death, after adjusting for age, gender, smoking, drinking, physical activity, uric acid, high-sensitivity C-reactive protein, dietary factors and carotid atherosclerosis status.
The carriers of the PNPLA3I148M variant also have a 3 times higher risk for the presence of metabolic syndrome (OR 2.939, 95% CI: 1.590-5.434, p=0.001) and a 2.1-fold higher risk for the presence of insulin resistance (OR 2.127, 95% CI: 1.078-4.194, p=0.029).
According to RETN +62G>A polymorphism, carriers with the A allele (GA/AA) had significantly increased resistin levels than subjects with the GG genotype, consequently, the RETN +62G>A polymorphism was found to be related to MS, biochemical parameters and anthropometric variables.
Together, our observations point to DDR2 as a hitherto unrecognized molecular link between metabolic syndrome and arterial fibrosis, and hence a therapeutic target.
This was accompanied with predomination of IL-10 over pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17) in the sera as well as Gal-3 over TNF-α and IL-17 in feces of UC patients with MetS.
This was accompanied with predomination of IL-10 over pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17) in the sera as well as Gal-3 over TNF-α and IL-17 in feces of UC patients with MetS.
Local dominance of Gal-3 and IL-10 over pro-inflammatory mediators in patients with MetS may present a mechanism for limiting the inflammatory process and subsequent tissue damage in UC.
This was accompanied with predomination of IL-10 over pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17) in the sera as well as Gal-3 over TNF-α and IL-17 in feces of UC patients with MetS.
Local dominance of Gal-3 and IL-10 over pro-inflammatory mediators in patients with MetS may present a mechanism for limiting the inflammatory process and subsequent tissue damage in UC.
The main factors associated with IR were body fat percentage and triglycerides; SNP for the ABCA1 gene was related to MS, obesity and low HDL-C; SNP for GCKR gene was related to high fasting glycemia, while APOAV SNP was related with MS, hypertriglyceridemia and low HDL-C. Our findings show that the Mexican genetic predisposition to NCD affects young adults, who can suffer MS, obesity and IR.
The main factors associated with IR were body fat percentage and triglycerides; SNP for the ABCA1 gene was related to MS, obesity and low HDL-C; SNP for GCKR gene was related to high fasting glycemia, while APOAV SNP was related with MS, hypertriglyceridemia and low HDL-C. Our findings show that the Mexican genetic predisposition to NCD affects young adults, who can suffer MS, obesity and IR.